Attique Iqra, Haider Zahra, Khan Maha, Hassan Samina, Soliman Mohamed Mohamed, Ibrahim Wisam Nabeel, Anjum Sumaira
Department of Biotechnology, Kinnaird College for Women University, Lahore, Pakistan.
Department of Biotechnology, Lahore College for Women University, Lahore, Pakistan.
Cancer Med. 2025 May;14(10):e70947. doi: 10.1002/cam4.70947.
Reactive oxygen species (ROS), a class of highly reactive molecules, are closely linked to the pathogenesis of various cancers. While ROS primarily originate from normal cellular processes, external stimuli can also contribute to their production. Cancer cells typically exhibit elevated ROS levels due to disrupted redox homeostasis, characterized by an imbalance between antioxidant and oxidant species. ROS play a dual role in cancer biology: at moderate levels, they facilitate tumor progression by regulating oncogenes and tumor suppressor genes, inducing mutations, promoting proliferation, extracellular matrix remodeling, invasion, immune modulation, and angiogenesis. However, excessive ROS levels can cause cellular damage and initiate apoptosis, necroptosis, or ferroptosis.
This review explores molecular targets involved in redox homeostasis dysregulation and examines the impact of ROS on the tumor microenvironment (TME). Literature from recent in vitro and in vivo studies was analyzed to assess how ROS modulation contributes to cancer development and therapy.
Findings indicate that ROS influence cancer progression through various pathways and cellular mechanisms. Targeting ROS synthesis or enhancing ROS accumulation in tumor cells has shown promising anticancer effects. These therapeutic strategies exhibit significant potential to impair tumor growth while also interacting with elements of the TME.
The ROS serve as both promoters and suppressors of cancer depending on their intracellular concentration. Their complex role offers valuable opportunities for targeted cancer therapies. While challenges remain in precisely modulating ROS for therapeutic benefit, they hold promise as synergistic agents alongside conventional treatments, opening new avenues in cancer management.
活性氧（ROS）是一类高反应性分子，与多种癌症的发病机制密切相关。虽然ROS主要源自正常细胞过程，但外部刺激也可促使其产生。由于氧化还原稳态被破坏，癌细胞通常表现出较高的ROS水平，其特征是抗氧化剂和氧化剂之间失衡。ROS在癌症生物学中发挥双重作用：在适度水平时，它们通过调节癌基因和肿瘤抑制基因、诱导突变、促进增殖、细胞外基质重塑、侵袭、免疫调节和血管生成来促进肿瘤进展。然而，过量的ROS水平可导致细胞损伤并引发凋亡、坏死性凋亡或铁死亡。
本综述探讨了参与氧化还原稳态失调的分子靶点，并研究了ROS对肿瘤微环境（TME）的影响。分析了近期体外和体内研究的文献，以评估ROS调节如何影响癌症发展和治疗。
研究结果表明，ROS通过多种途径和细胞机制影响癌症进展。靶向ROS合成或增强肿瘤细胞中的ROS积累已显示出有前景的抗癌效果。这些治疗策略在抑制肿瘤生长以及与TME成分相互作用方面具有显著潜力。
根据细胞内浓度，ROS既可以是癌症的促进剂，也可以是抑制剂。它们的复杂作用为靶向癌症治疗提供了宝贵机会。虽然在精确调节ROS以获得治疗益处方面仍存在挑战，但它们有望作为与传统治疗协同的药物，为癌症管理开辟新途径。
